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Simple Generation of a High Yield Culture of Induced Neurons from Human Adult Skin Fibroblasts
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Direct Reprogramming Rather than iPSC-Based Reprogramming Maintains Aging Hallmarks in Human Motor Neurons.
Yu Tang1,2,3, Meng-Lu Liu1,2, Tong Zang1,2
1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Frontiers in Molecular Neuroscience
|November 23, 2017
Summary
Directly reprogramming motor neurons (MNs) from aged fibroblasts preserves aging hallmarks, unlike induced pluripotent stem cells (iPSCs) which rejuvenate. Directly converted MNs are thus better for modeling age-related motor neuron diseases (MNDs).
Area of Science:
- Neuroscience
- Stem Cell Biology
- Aging Research
Background:
- Motor neuron diseases (MNDs) like ALS are linked to aging.
- Modeling age-related neurodegeneration requires cells that retain aging characteristics.
- Induced pluripotent stem cells (iPSCs) and direct reprogramming are key methods for generating motor neurons (MNs).
Purpose of the Study:
- To compare the aging status of MNs derived from iPSCs versus directly reprogrammed fibroblasts.
- To determine which method better recapitulates age-related features for modeling MNDs.
Main Methods:
- Generated MNs from human iPSCs and primary fibroblasts using transcription factors.
- Assessed aging hallmarks including telomere length, senescence, DNA damage, heterochromatin loss, and SA-β-Gal activity.
- Compared aging markers between iPSC-derived MNs and directly reprogrammed MNs.
Main Results:
- Human iPSCs reset aging features like telomere attrition and senescence.
- Directly reprogrammed MNs retained aging hallmarks from old donors (DNA damage, heterochromatin loss, SA-β-Gal activity).
- iPSC-derived MNs did not maintain donor aging characteristics.
Conclusions:
- iPSC-based models undergo rejuvenation, losing age-related memories.
- Direct reprogramming maintains aging features, making these MNs more suitable for modeling late-onset MND pathogenesis.
- Directly reprogrammed MNs offer a more accurate model for studying age-associated neurodegenerative diseases.
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